Identification of quantitative trait loci controlling partial clubroot resistance in new mapping populations of Arabidopsis thaliana

2008 ◽  
Vol 117 (2) ◽  
pp. 191-202 ◽  
Author(s):  
Mélanie Jubault ◽  
Christine Lariagon ◽  
Matthieu Simon ◽  
Régine Delourme ◽  
Maria J. Manzanares-Dauleux
2009 ◽  
Vol 184 (1) ◽  
pp. 180-192 ◽  
Author(s):  
Artak Ghandilyan ◽  
Luis Barboza ◽  
Sébastien Tisné ◽  
Christine Granier ◽  
Matthieu Reymond ◽  
...  

PLoS ONE ◽  
2011 ◽  
Vol 6 (6) ◽  
pp. e20886 ◽  
Author(s):  
Rebecca A. Silady ◽  
Sigi Effgen ◽  
Maarten Koornneef ◽  
Matthieu Reymond

2008 ◽  
Vol 21 (2) ◽  
pp. 198-207 ◽  
Author(s):  
Ophélie Sicard ◽  
Olivier Loudet ◽  
Joost J. B. Keurentjes ◽  
Thierry Candresse ◽  
Olivier Le Gall ◽  
...  

In compatible interactions between plants and viruses that result in systemic infection, symptom development is a major phenotypic trait. However, host determinants governing this trait are mostly unknown, and the mechanisms underlying it are still poorly understood. In a previous study on the Arabidopsis thaliana–Plum pox virus (PPV) pathosystem, we showed a large degree of variation in symptom development among susceptible accessions. In particular, Cvi-1 (Cape Verde islands) accumulates viral particules but remains symptomless, Col-0 (Columbia) sometimes shows weak symptoms compared with Ler (Landsberg erecta), which always shows severe symptoms. Genetic analyses of Col × Ler and Cvi × Ler F2 and recombinant inbred line (RIL) populations suggested that symptom development as well as viral accumulation traits are polygenic and quantitative. Three of the symptom quantitative trait loci (QTL) identified could be confirmed in near-isogenic lines, including PSI1 (PPV symptom induction 1), which was identified on the distal part of chromosome 1 in both RIL populations. With respect to viral accumulation, several factors have been detected and, interestingly, in the Col × Ler population, two out of three viral accumulation QTL colocalized with loci controlling symptom development, although correlation analysis showed weak linearity between symptom severity and virus accumulation. In addition, in the Cvi × Ler RIL population, a digenic recessive determinant controlling PPV infection was identified.


2006 ◽  
Vol 57 (6) ◽  
pp. 1363-1372 ◽  
Author(s):  
Virginia M. C. Luquez ◽  
Yamila Sasal ◽  
Micaela Medrano ◽  
María I. Martín ◽  
Mercedes Mujica ◽  
...  

2010 ◽  
Vol 23 (1) ◽  
pp. 91-102 ◽  
Author(s):  
Reza Aghnoum ◽  
Thierry C. Marcel ◽  
Annika Johrde ◽  
Nicola Pecchioni ◽  
Patrick Schweizer ◽  
...  

The basal resistance of barley to powdery mildew (Blumeria graminis f. sp. hordei) is a quantitatively inherited trait that is based on nonhypersensitive mechanisms of defense. A functional genomic approach indicates that many plant candidate genes are involved in the defense against formation of fungal haustoria. It is not known which of these candidate genes have allelic variation that contributes to the natural variation in powdery mildew resistance, because many of them may be highly conserved within the barley species and may act downstream of the basal resistance reaction. Twenty-two expressed sequence tag or cDNA clone sequences that are likely to play a role in the barley–Blumeria interaction based on transcriptional profiling, gene silencing, or overexpression data, as well as mlo, Ror1, and Ror2, were mapped and considered candidate genes for contribution to basal resistance. We mapped the quantitative trait loci (QTL) for powdery mildew resistance in six mapping populations of barley at seedling and adult plant stages and developed an improved high-density integrated genetic map containing 6,990 markers for comparing QTL and candidate gene positions over mapping populations. We mapped 12 QTL at seedling stage and 13 QTL at adult plant stage, of which four were in common between the two developmental stages. Six of the candidate genes showed coincidence in their map positions with the QTL identified for basal resistance to powdery mildew. This co-localization justifies giving priority to those six candidate genes to validate them as being responsible for the phenotypic effects of the QTL for basal resistance.


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